1) ARE REGULATORY T CELLS BEING EXHAUSTED BY EXPOSURE TO THE SPIKE PROTEIN SUPERALLERGEN IN SEVERE COVID?

There has been much discussion of immune dysregulation in COVID-19 disease. One of the most interesting recurring findings is CD8 T-Cell Exhaustion. CD8 T-Cells are
2) regulatory T-cells. What is most curious is that they become MORE exhausted the MORE severe the disease is.

I believe this is due to the increased presence and persistence of SPIKE PROTEINS.

If you look at LKB1, this liver kinase allows access to CHROMATIN (regulates
3) METASTASIS), MITOCHONDRIAL FUNCTION and T-REGS.

Spike Protein sequences interact with WIPI3/WDR45B. which are scaffolds of the LKB1 signalling circuits.

This may offer evidence that prolonged exposure to the spike protein is behind the allergic/superallergen nature of
4) COVID.

In a referenced study below, the role and mechanism of pterostilbene (Pts) in mast cell degranulation in vitro and in vivo were investigated. The results showed that Pts inhibited mast cell-mediated local passive allergic reactions in mice. In addition, treatment with
5) Pts reduced both histamine release and calcium influx in rat peritoneal mast cells and RBL-2H3 cells and reduced IgE-mediated mast cell activation. Furthermore, the mechanism underlying Pts inhibition of mast cell signaling was probed via studying the effects of Pts on liver
6) kinase B1 (LKB1), including the use of the LKB1 activator metformin and siRNA knockdown of LKB1. The data showed that Pts reduced the release of inflammatory mediators such as tumor necrosis factor-α, interleukin-6, leukotriene C4, and prostaglandin D2 in mast cells by
7) activating the LKB1/adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway. Furthermore, Pts inhibited phosphorylation of FcεRI and FcεRI-mediated degranulation in RBL-2H3 cells. These effects were attenuated after LKB1 knockdown. Taken together, Pts
8) could inhibit FcεRI signaling through activation of the LKB1/AMPK signaling pathway in IgE-mediated mast cell activation. Thus, Pts might be an effective therapeutic agent for mast cell-mediated allergic diseases.

pubs.acs.org/doi/10.1021/ac…

biorxiv.org/content/10.110…
10) Mice with a Treg-specific deletion of LKB1 developed a fatal inflammatory disease characterized by excessive TH2-type-dominant responses. LKB1 deficiency disrupted Treg cell survival and mitochondrial fitness and metabolism, but also induced aberrant expression of immune
11) regulatory molecules including the negative co-receptor PD-1 and the TNF receptor superfamily proteins GITR and OX40.

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More from @Parsifaler

2 Jul
1) LKB1, MASTER COVID SPECTRE: FROM CARCINOGENESIS TO METABOLISM, AM DYSFUNCTION AND SKELETAL MUSCLE HOMEOSTASIS

I believe without question the spike protein is downregulating/"turning off" expression of LKB1. At first glance, the most immediate danger is carcinogenesis Image
2) as it was found that loss of Lkb1 was sufficient to drive the initial steps of carcinogenesis ex vivo.

Lkb1 plays an important role in regulating glucose homeostasis and energy metabolism. In addition, there is also evidence that has highlighted a prominent role for Lkb1 in
3) the function of macrophages. Lkb1 inhibits the activation and inflammatory function of innate macrophages. It was found that disruption of Lkb1 impaired the self-renewal of AMs, contributing to the reduction of AMs, which led to aggravated symptoms and EXCESSIVE accumulation
Read 8 tweets
2 Jul
1) METABOLICALLY INDUCED IMMUNE DEFICIENCY

Given the mitcochondrial dysfunction obeserved in COVID-19, I have turned my attention towards liver kinase B1 (LKB1). This kinase is intimately involved with both ATP production, T-cell development, peripheral T-cell homeostasis, and Image
2) T-cell effector function.

I believe SARS-CoV-2 is epigenetically impairing LKB1. LKB1-deficient T cells exhibited defects in cell proliferation and viability and altered glycolytic and lipid metabolism. Interestingly, loss of LKB1 promoted increased T cell activation and Image
3) inflammatory cytokine production by both CD4+ and CD8+ T cells.

LKB1 was recently found to have prominent roles in hematopoietic stem cell viability and renewal, suggesting a prominent function for LKB1 in hematopoietic cells. These features are also observed in COVID-19.
Read 8 tweets
1 Jul
1) LKB1: THE STAR OF THE SHOW IS STILL WAITING IN THE WINGS: HOW HAVE WE MISSED THIS?

Endothelial Cell-Specific LKB1 Deletion Causes Endothelial Dysfunction and Hypertension in Mice in vivo

The gene, also known as STK11, is involved in controlling blood sugar levels.

LKB1 Image
2) programs the metabolic and functional fitness of Treg cells in the control of immune tolerance and homeostasis. Mice with a Treg-specific deletion of LKB1 developed a fatal inflammatory disease characterized by excessive TH2-type-dominant responses. LKB1 deficiency disrupted
3) Treg cell survival and mitochondrial fitness and metabolism, but also induced aberrant expression of immune regulatory molecules including the negative co-receptor PD-1 and the TNF receptor superfamily proteins GITR and OX40. The results point to functional exhaustion of Treg
Read 9 tweets
30 Jun
1) I am looking for the source study, will post once I find. This sounds completely legit:

This analysis by epidemiologist Jessica Rose, PhD, from Canada, indicates that the vax injury syndromes appear to fall into three major categories: neurological, cardiovascular/
2) thromboembolic, and immunological. Because some individuals must get a more substantial distribution and uptake of the mRNA or adenoviral DNA, wherever the density of spike protein generation occurs determines what organ is going to be most prominently injured. To think
3) developers would use genetic platforms coding for NORMAL genes and turn them into delivery vehicles for the code of dangerous SPIKE protein is the most colossal biotech error in the history of medicine. Those working on mRNA had visions of the Nobel prize, while they really
Read 5 tweets
30 Jun
1) 2007 PEPTIDE SHARING STUDY: THE GARROTING OF THE HUMAN IMMUNE SYSTEM

Antibodies against these (spike protein) motifs may contain NEUTRALIZATION activity against SARS-CoV infection OR PARTICIPATE in the immunopathogenesis induced by SARS-CoV.

I believe the massive peptide
2) sharing of the spike protein with human peptides is the elephant in the room - and the one that spike protein therapy developers is, at this point, purposefully ignoring.

In 2007 it was discovered that there was peptide sharing between four pathogenic regions of SARS-CoV
3) S protein which share sequence homology with different human proteins. This was determined to be DOUBLE EDGED. Neutralization OR immunopathogenesis.

Therefore, if immunopathogensis is occurring because of the peptide sharing, then each subsequent exposure of the host to the
Read 5 tweets
29 Jun
1) SPIKE PROTEIN DISPLAYED ON CELL MEMBRANE THEN CLEAVED: PRIONS, FERROPORTIN, THE BLOOD BRAIN BARRIER AND HEPCIDIN

Concerning iron dysmetabolism in COVID-19, Ehsani has highlighted a remarkable similarity between the distant amino acid sequence of SARS-CoV-2 spike glycoprotein
2) cytoplasmic tail and the hepcidin protein.
Coronaviruses recognize host receptors using their spike proteins, facilitating conformation transition, so to bind cell membrane and enter host cytoplasm; by using host furins and proteases, coronaviruses may cleave their spike
3) polypeptides, thus favoring the cell entry. The found hepcidin mimicry by the virus would take place through this complex mechanism.

Perhaps the reason we are seeing strokes, blindness and other neurodegenerative activity post spike protein therapies is that that ferroportin
Read 5 tweets

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